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CURRENT Diagnosis & Treatment in Cardiology > Chapter 9. Mitral Stenosis >

Essentials of Diagnosis

  • Exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, or fatigue (later stages).
  • Opening snap, loud S1 (closing snap), diastolic rumbling murmur; with pulmonary hypertension, a parasternal lift with a loud P2.
  • ECG evidence of left atrial enlargement or atrial fibrillation; right ventricular hypertrophy in later stages.
  • Chest radiographic signs of left atrial enlargement and normal left ventricular size.
  • Thickened mitral valve leaflets with restricted valve motion and reduced orifice area demonstrated on two-dimensional echocardiography.
  • An elevated transmitral pressure gradient and prolonged pressure half-time by Doppler echocardiography.

General Considerations

The normal mitral apparatus is a complex structure whose components must permit a large volume of blood to pass from the left atrium to the left ventricle. The cross-sectional area of a normal mitral valve ranges from 4 cm2 to 6 cm2 in an adult and a transmitral pressure gradient develops when the valve is narrowed to < 2.5 cm2. Left atrial pressures begin to rise and are transmitted to the pulmonary vasculature and right side of the heart. Several congenital and acquired conditions result in impaired filling of the left ventricle and may be confused with mitral stenosis (Table 9–1).

Table 9–1. Conditions Causing Left Ventricular Inflow Obstruction.

Congenital

   

Valvular mitral stenosis

   

Subvalvular ring

   

Cor triatriatum

   

Pulmonary vein stenosis

Acquired

   

Valvular mitral stenosis

   

Atrial myxoma

   

Thrombus

   

Neoplasm

   

Large fungal or bacterial vegetation

   

Prosthetic valve dysfunction

The predominant cause of mitral stenosis in adults is rheumatic involvement of the mitral valve and approximately two-thirds of all patients with rheumatic mitral stenosis are female. However, a large proportion of patients with rheumatic valve disease—nearly 50%—have no history of rheumatic fever. Other causes of mitral stenosis are extremely rare. These figures will most likely change due to the impressive reduction of rheumatic fever in developed countries, although rheumatic fever remains a problem in developing countries and most likely reflects the reduced availability of antibiotics and the virulence of the strains of Streptococcus.

Acute rheumatic fever may produce a pancarditis involving the endocardium, myocardium, and pericardium. Aschoff bodies in the myocardium are very specific for a history of rheumatic carditis. Involvement of the mitral valve apparatus is the rule and may produce fusion and thickening of the commissures, cusps, and chordae tendineae. In addition, the fibrosis and calcification of the leaflets may extend to the valve ring. It is still debatable if the progression of mitral stenosis is due to a smoldering rheumatic process and recurrent infections or the constant trauma of turbulent flow produced by a deformed valve.

As the stenosis progresses, a transmitral pressure gradient develops to facilitate flow across the stenotic valve in diastole. Furthermore, the atrial contraction may augment this diastolic pressure gradient (assuming the heart is in normal sinus rhythm). Both the mitral valvular gradient (MVG) and mitral valvular flow (MVF) are required to assess the mitral valve area (MVA) as expressed by the Gorlin formula:

The mitral valvular flow is a function of cardiac output and heart rate. An increase in cardiac output or heart rate will increase the transmitral flow. As expressed by the Gorlin formula, the increased mitral valvular flow (produced by an increased cardiac output or tachycardia) elevates the mitral valvular gradient exponentially assuming the mitral valve area remains constant. The increased mitral valvular gradient produces an elevated left atrial pressure. This is an important concept for the development of symptoms.

Essop MR et al. Rheumatic and nonrheumatic valvular heart disease: epidemiology, management and prevention in Africa. Circulation. 2005 Dec 6;112(23):3584–91. [PMID: 16330700]

Clinical Findings

Symptoms and Signs

Early in the disease, patients may be asymptomatic. However, conditions that increase cardiac output or heart rate will increase the mitral valvular gradient and left atrial pressure as described earlier. The elevated left atrial pressure is subsequently transmitted into the pulmonary circulation, leading to dyspnea, and may facilitate the early diagnosis of mitral stenosis. Common conditions that increase cardiac output or heart rate are exercise, hyperthyroidism, pregnancy, atrial fibrillation, and fever. In addition, venous return is augmented in the supine position and may produce orthopnea and paroxysmal nocturnal dyspnea in patients with moderate disease.

As the disease progresses, the pulmonary artery pressure increases proportionally to the pulmonary capillary pressure. The proportional increase is termed “passive pulmonary hypertension” because the increased pressure produced by the right ventricle is required to drive blood across the pulmonary vascular bed into the left atrium. In some patients with severe mitral stenosis, the pulmonary artery pressure is increased disproportionally to the pulmonary capillary pressure. The disproportional increase is termed “reactive pulmonary hypertension.” The reactive pulmonary hypertension is secondary to pulmonary artery constriction and organic obliterative changes in the pulmonary vascular bed. These changes typically produce symptoms of right-heart failure and may not be completely reversible.

The mitral valve stenosis and atrial inflammation secondary to rheumatic fever may produce dilatation and postinflammatory changes of the left atrium. These changes predispose the patient to palpitations and atrial fibrillation. In addition, there is an increased risk of systemic embolization resulting in a stroke, myocardial infarction (coronary embolism), splenic or renal infarction, and peripheral artery occlusion. For patients in sinus rhythm, age, the presence of a left atrial thrombus, mitral valve area, and the presence of significant aortic regurgitation are positively associated with embolism. In cases of atrial fibrillation, previous embolism is positively associated with embolism; percutaneous balloon mitral commissurotomy is a negative predictor. Spontaneous echo contrast (also known as smoke) detected by transesophageal echocardiography is associated with systemic embolism. Most emboli appear to originate from the left atrium, especially the left atrial appendage.

Increased pulmonary pressures and vascular congestion produce hemoptysis. Hemoptysis may present as a sudden hemorrhage (termed “pulmonary apoplexy”; this condition is rarely life-threatening), pink frothy sputum resulting from pulmonary edema, blood-tinged sputum associated with dyspnea or bronchitis, and pulmonary infarction due to a pulmonary embolism. Chest pain may develop and resembles angina. The chest pain is most likely the result of pulmonary hypertension and right ventricle hypertrophy and is typically relieved with correction of the mitral stenosis, although concomitant coronary artery disease should be evaluated with the development of chest pain. Endocarditis is primarily associated with mild mitral stenosis and is quite unusual with calcification in severe mitral stenosis.

Physical Examination

The general appearance of patients with mitral stenosis is usually unremarkable. Older studies reported mitral facies, which is characterized by pinkish-purple patches on the cheeks produced by low cardiac output, systemic vasoconstriction, and right-sided heart failure. This sign is now extremely rare. Right-sided heart failure also produces an elevated jugular venous pulse with a prominent a wave (assuming the heart is in normal sinus rhythm) and v wave (produced by tricuspid regurgitation).

The apical impulse is generally normal or decreased, representing normal left ventricular function and decreased left ventricular volume. Palpation of the S1 over the precordium is a pathognomonic finding and suggests that the anterior mitral valve leaflet is pliable. When the patient is in the left lateral decubitus position, a diastolic thrill may be appreciated. When pulmonary hypertension is present, a parasternal right ventricular heave develops along with a palpable P2.

Auscultation of the heart sounds may reveal an accentuated S1 early in the disease. Accentuation of S1 occurs when the left ventricular pressure rises rapidly in early systole, and the flexible mitral valve leaflets transgress a wide closing excursion. As the severity of mitral stenosis increases with calcification and fibrosis of the leaflets, the amplitude of S1 subsequently diminishes. When pulmonary hypertension is present, the splitting of the second heart sound may narrow and become a single accentuated S2. An S3 originating from the left ventricle is absent in patients with mitral stenosis unless there is concomitant coronary artery disease, mitral regurgitation, or aortic regurgitation. An S4, if present, originates from the right ventricle when it is hypertrophied and dilated secondary to pulmonary hypertension.

The opening snap is due to sudden tensing of the valve leaflets after they have completed their opening excursion. The vigorous opening of the leaflets is secondary to high left atrial pressures accompanied by a fall in left ventricular pressures in early diastole. The opening snap is audible (high frequency) at the apex, using the diaphragm of the stethoscope.

It is imperative to examine the patient in the left lateral decubitus position for a diastolic murmur. In addition, the murmur may be accentuated by having the patient exercise prior to auscultation. The murmur is described as a rumble (low frequency) and is audible at the apex, using the bell of the stethoscope. The diastolic murmur of mitral stenosis reflects the mitral valvular gradient and the duration of blood flow across the valve. In mild mitral stenosis, the early diastolic decrescendo murmur is brief and is accompanied by a presystolic murmur. The presystolic murmur is secondary to the gradient produced by the atrial contraction. However, the presystolic murmur may be produced in atrial fibrillation and is due to the narrowing of the mitral orifice produced by ventricular systole prior to S1. A murmur of pulmonary regurgitation (Graham Steell murmur) may be present and difficult to distinguish from the murmur of aortic regurgitation.

Reliable indicators of the severity of mitral stenosis are the A2–OS interval and the length (rather than intensity) of the diastolic murmur. As the severity of mitral stenosis increases, the A2–OS interval decreases and the length of the murmur increases. The decreased interval is the result of increased left atrial pressures, producing a mitral valvular gradient at the very onset of diastole. The gradient leads to an early excursion of the valve leaflets (early OS) and continues throughout all of diastole (pandiastolic murmur). The opening snap and murmur may become inaudible when mitral stenosis is very severe and the valve leaflets are rigid.

Diagnostic Studies

Electrocardiography

Early in the disease, the electrocardiogram (ECG) typically reveals a normal sinus rhythm and is very insensitive. As the disease progresses, left atrial enlargement leads to changes in the P wave. The P wave in lead II becomes broad and notched (termed “P-mitrale”) along with a prominent terminal component of the P wave in lead V1. The P wave axis migrates between +45 and –30 degrees. Atrial fibrillation subsequently develops in many patients, and the previously described findings are lost. As the pulmonary hypertension becomes severe (70–100 mm Hg), right axis deviation develops in addition to an R wave greater than the S wave in lead V1. In pure mitral stenosis, left ventricular hypertrophy is absent.

Chest Radiography

Radiologic examination of the cardiac silhouette is quite advantageous. Left atrial enlargement may produce a “double-density,” straightening of the left heart border, along with elevation of the left mainstem bronchus (PA view), and impingement on the esophagus due to posterior extension (lateral view). Right ventricular enlargement may occupy the retrosternal space (lateral view). The left ventricular silhouette is normal in pure mitral stenosis, and calcification of the mitral valve is difficult to see on routine chest radiograph. Radiologic examination of the lung fields reveals elevated pulmonary pressures. The pulmonary arteries are prominent, and blood flow is redistributed to the upper lobes (cephalization). Transudation of fluid into the interstitium occurs, resulting in Kerley A lines, Kerley B lines, and pulmonary edema.

Echocardiography

The echocardiographic examination is now the keystone of the diagnostic assessment of mitral stenosis. Valuable information is provided with the following echocardiographic techniques: M-mode, two-dimensional, three-dimensional, Doppler, stress, and transesophageal echocardiography (TEE).

M-Mode

As mitral stenosis progresses, the usual M-shaped configuration of the anterior mitral leaflet is altered. The diastolic posterior motion of the anterior leaflet is reduced, producing a reduced E-F slope. In patients in sinus rhythm, the A wave, which is normally seen with an atrial contraction, may be reduced or absent. Fusion of the commissures produces a concordant motion of the anterior and posterior mitral leaflets. Although this mode of echocardiography can provide a qualitative diagnosis, it is the least reliable means of quantifying the severity of obstruction.

Two-Dimensional Echocardiography

This method provides a more complete view of the mitral valve apparatus. The parasternal long axis may reveal diastolic “doming” of the mitral valve and a “hockey stick” configuration of the anterior leaflet. Pliable leaflets with restricted mobility of the leaflet tips produce this configuration. The parasternal short axis can image the orifice of the mitral valve that demonstrates the typical “fish mouth” configuration. After visualization, the orifice is planimetered in diastole to obtain an accurate measurement of the mitral valve area. This measurement is very reliable but may be operator-dependent and prone to error. The inaccuracy is further evident after commissurotomy due to the distortion produced by commissural splitting. With the advent of percutaneous mitral balloon valvotomy (PMBV), the mitral apparatus morphology determined by two-dimensional echocardiography plays an extremely important role for selection criteria.

Three-Dimensional Echocardiography

Three-dimensional echocardiography can be used to assess mitral valve area via planimetry. The three-dimensional nature helps optimize the plane of the mitral valve. This technique has been demonstrated to be as accurate as other methods for determining mitral valve area. It is limited in the ability of the transducer to obtain adequate images.

Transesophageal Echocardiography

TEE is useful in assessing the left atrium prior to PMBV. It assists with the detection of left atrial thrombi and spontaneous echocardiographic contrast (smoke). It is extremely useful in assessing mitral valve commissural morphology to help guide optimal management in patients undergoing evaluation for balloon mitral valvotomy. Its use, especially with three-dimensional echocardiography, in assessing mitral valve area is less clear. Planimetry of the proper mitral valve plane for mitral stenosis is more difficult with this technique.

Doppler Echocardiography

Doppler accurately assesses the hemodynamic effects of the mitral valve stenosis; the indicators are mitral valvular gradient, mitral valve area, and pulmonary artery pressures. The mitral valvular gradient is measured by obtaining the velocity of mitral inflow. The velocity (V) is converted to the pressure gradient between the atrium and ventricle using the modified Bernoulli equation:

The mitral valve area can be estimated using the pressure half-time method, the proximal isovelocity surface area (PISA), or the continuity of flow method. The pressure half-time is currently the most widely used technique for estimating the mitral valve area from Doppler-derived data. The pressure half-time is the time required for the peak pressure gradient between the left atrium and the left ventricle to decline to one-half of its original value. Doppler velocity is converted into a pressure gradient by dividing the initial flow velocity by the square root of 2. Empirically, a pressure half-time of 220 ms correlates with a mitral valve area of 1 cm2.

As the mitral valve area decreases, the pressure half-time increases. However, the pressure half-time may be inaccurate in patients with abnormalities of left atrial or left ventricular compliance, those with associated aortic regurgitation, and those with a previous mitral valvotomy. In addition, the presence of severe mitral regurgitation appears to underestimate mitral valve area by pressure half-time. The PISA and the continuity of flow method provide more accurate estimates of mitral valve area in these circumstances but are rarely used in clinical practice.

Pulmonary artery pressures are determined using continuous wave Doppler. The velocity of tricuspid regurgitation produced by pulmonary hypertension is measured, yielding a gradient between the right atrium and right ventricle with the use of the modified Bernoulli equation described previously. The right ventricular systolic pressure is obtained by adding the estimated right atrial pressure to the gradient.

Use of tissue Doppler imaging can also be used in monitoring mitral stenosis. Specifically, measurements of the isovolumetric relaxation time (IVRT), mitral inflow velocity (E), and annular early diastolic velocity (Ea) can be followed annually, especially after PMBV, to assess left ventricular filling pressure. This is especially useful in tracking patients after valve intervention.

Stress Echocardiography

Dobutamine stress echocardiography (DSE) and exercise echocardiography are also used to assess valve function. With DSE, development of a mean mitral valve gradient of greater than 18 mm Hg demonstrates high-risk patients. Exercise echocardiography can be used to demonstrate increased pulmonary artery pressures with exercise to help determine who would benefit from early intervention, such as valvotomy or valve replacement.

Each method has several limitations, and it is imperative to achieve cross validation. In most instances, measurements of the mitral valvular gradient, mitral valve area, and pulmonary artery pressures correlate well with one another with the use of a transthoracic echocardiogram. If correlation does not occur, a cardiac catheterization, TEE, three-dimensional echocardiogram, or exercise with simultaneous Doppler estimation of the transmitral and pulmonary pressures should be sought to clarify inconsistencies. In addition, a TEE can assess the presence or absence of left atrial thrombus in patients being considered for PMBV or cardioversion.

Cardiac Catheterization

Direct measurements of left atrial and left ventricular pressures require a transseptal catheterization and predispose the patient to unnecessary risks. Conventional cardiac catheterization uses the pulmonary capillary wedge pressure for indirect measurement of left atrial pressures. Although the pulmonary capillary wedge accurately reflects the mean left atrial pressure, it overestimates the transmitral gradient. Presently, cardiac catheterization has a very limited role in determining the severity of mitral stenosis due to the recent advances in echocardiography.

Magnetic Resonance Imaging

MRI has been shown to be accurate in determining mitral valve area. Two different methods of MRI can be used. Three-dimensional reconstruction can accurately determine mitral valve area compared with echocardiography and Doppler pressure half-time. In addition, velocity encoded cardiovascular magnetic resonance (VE-CMR) compares favorably with Doppler in determining pressure half-time and calculating mitral valve area.

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Djavidani B et al. Planimetry of mitral valve stenosis by magnetic resonance imaging. J Am Coll Cardiol. 2005 Jun 21;45(12):2048–53. [PMID: 15963408]

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Hildick-Smith DJ et al. Pulmonary capillary wedge pressure in mitral stenosis accurately reflects mean left atrial pressure but overestimates transmitral gradient. Am J Cardiol. 2000 Feb 15;85(4):512–5. [PMID: 10728964]

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Treatment

Medical Therapy

Primary prophylaxis consists of an early diagnosis of group A streptococcal pharyngitis. Treatment started within 7–9 days after onset of illness may prevent rheumatic fever. Secondary prophylaxis may be individually tailored, but there are no firm guidelines. Recurrence of rheumatic fever is more common in young patients and in patients in whom carditis developed during the initial episode. Therefore, with carditis, secondary prevention continues for 10 years or until age 25. Without carditis, secondary prevention continues for 5 years or until age 18. The prevention of repeated attacks may delay the progression of mitral stenosis.

Patients with mitral stenosis are considered to be at moderate risk for bacterial endocarditis. Therefore, endocarditis prophylaxis was recommended for certain procedures specified by older guidelines. However, there is a recent debate concerning whether dental procedures predispose to endocarditis and whether antibiotic prophylaxis is of any value; current guidelines do not recommend antibiotic prophylaxis for mitral stenosis. The choice of antibiotics to treat endocarditis may be further complicated if the patient is receiving penicillin for prophylaxis against rheumatic fever. Resistance to penicillin and cephalosporins may develop in this scenario, and an alternative antibiotic should be given for prophylaxis against endocarditis.

Medical management of mitral stenosis with normal sinus rhythm is limited. A benefit is derived from salt restriction and diuretics when there is evidence of pulmonary vascular congestion. Digitalis does not benefit patients in sinus rhythm unless an associated left ventricular dysfunction is present. -Blockers can significantly decrease heart rate and cardiac output. The decreased heart rate and cardiac output subsequently lead to a decrease in the transmitral gradient. Although there appears to be a physiologic advantage with the use of -blockers, the data are conflicting. -Blockers may be reserved for patients who have exertional symptoms if the symptoms occur at high heart rates. Anticoagulation is beneficial for cases with normal sinus rhythm with a prior embolic event or a left atrial dimension > 55 mm Hg by echocardiography.

Medical management of mitral stenosis and atrial fibrillation can alleviate a variety of complications. Atrial fibrillation in patients with mitral stenosis is poorly tolerated due to a loss of atrial contraction and an associated rapid ventricular rate. The rate control is achieved by using a -blocker, calcium channel blocker, or digitalis. Electrical or chemical cardioversion should be performed with appropriate anticoagulation. Class IA, IC, and III agents can be used to terminate acute-onset atrial fibrillation and prevent recurrences of atrial fibrillation. Most antiarrhythmics increase the likelihood of maintaining normal sinus rhythm to approximately 50–70% of patients per year after cardioversion. Amiodarone appears to be more effective than sotalol or propafenone, although the antiarrhythmic should be tailored to the patient because of the risks of side effects with each agent. Heart rate control is most commonly achieved with a combination of nondihydropine calcium channel blockers, -blockers, and digoxin. Anticoagulation is recommended for all patients who are unable to maintain normal sinus rhythm.

In pregnancy, the heart rate and cardiac output are increased substantially along with an increase in maternal blood volume. Nevertheless, most healthy pregnant women with mild to moderate mitral stenosis can be treated medically. Diuretics and -blockers appear to be safe for use in pregnancy. Quinidine or procainamide are the drugs of choice if an antiarrhythmic drug is needed to maintain normal sinus rhythm. If anticoagulation is necessary, warfarin should be avoided and the patient should be treated appropriately with heparin.

Percutaneous Mitral Balloon Valvotomy

PMBV involves a transseptal puncture during cardiac catheterization. The transseptal approach offers direct access to the mitral orifice, after which a single- or double-balloon commissurotomy is performed. The mechanism of action is primarily commissural splitting and fracture of calcium deposits that improve valvular function. The Inoue and double-balloon techniques produce similar long-term results.

Two newer approaches are gaining acceptance. The retrograde nontransseptal balloon mitral valvuloplasty is based on an externally steerable cardiac catheter that enters the left atrium retrograde via the left ventricle. This technique avoids the need for a transseptal puncture and dilatation of the interatrial septum. Balloon valvuloplasty is recommended in patients who are symptomatic, have moderate to severe mitral stenosis, have pliable leaflets, and do not have a left atrial thrombus or significant mitral regurgitation. Patients who are either asymptomatic but have severe mitral stenosis or are symptomatic but have high surgical risks are considered acceptable candidates for balloon valvuloplasty. It is not recommended in cases of mild mitral stenosis. Important baseline variables include operator experience, age, New York Heart Association (NYHA) functional class, atrial fibrillation, cardiothoracic index, echocardiographic score, mean pulmonary artery pressure, and mitral regurgitation. The underlying mitral valve morphology is the most important factor in determining outcome, and echocardiographic scoring systems have been developed for assessing the morphology.

Balloon valvotomy is especially useful in the younger population. Children do extremely well with this technique and avoid surgical replacement of the valve indefinitely. Repeat balloon valvotomy is well tolerated and provides good immediate results, but the long-term results are inferior to initial balloon valvotomy. There is increased restenosis, mitral regurgitation, and atrial fibrillation in this population.

Balloon valvotomy during pregnancy is extremely well tolerated. Women with severe symptomatic mitral stenosis safely undergo valvotomy with marked increases in mitral valve area. Fetal development is normal for most women undergoing this procedure.

Mitral balloon valvotomy does not prevent the development of atrial fibrillation. Patients may require the maze procedure in order to lessen the risk or the development of atrial fibrillation.

Surgical Therapy

Three surgical approaches are used to treat mitral stenosis: closed commissurotomy, open commissurotomy, and mitral valve replacement. A closed commissurotomy is performed without the aid of a cardiopulmonary bypass. The surgeon enters the heart using either a transatrial or a transventricular approach. A dilator is subsequently introduced across the mitral valve without direct visualization. The lack of direct visualization is an obvious limitation, and patients are selected in a manner similar to that used for PMBV. Without cardiopulmonary bypass, the closed approach allows for a substantial reduction in cost compared with open commissurotomy and PMBV. Due to the substantial reduction of cost, closed commissurotomy is the procedure of choice in developing nations.

Open commissurotomy has several advantages over the closed procedure. Under direct visualization, the surgeon can incise commissures, débride calcium deposits, and separate fused chordae tendineae and the underlying papillary muscle. In addition, thrombi are removed from the left atrium, and many surgeons will amputate the left atrial appendage to remove a potential source of postoperative emboli. Open commissurotomy is usually preferred in patients with a left atrial thrombus or severe subvalvular and calcific disease; however, it is costly with the use of cardiopulmonary bypass.

Mitral valve replacement is primarily indicated for patients with moderate or severe mitral stenosis (mitral valve area < 1.5 cm2) and NYHA III–IV symptoms who are not considered candidates for PMBV or mitral repair. The choice of a mechanical valve versus a bioprosthetic should be individualized. A recent study suggested that there is no difference between the St. Jude and Medtronic Hall prosthesis with respect to late clinical performance or hemodynamic results. Therefore, the choice of mechanical valve should be based on the surgeon’s experience and preference. Mechanical valves offer durability and a larger effective orifice area than bioprosthetics; however, mechanical valves are more thrombogenic and require continuous anticoagulation. Although there is a lower frequency of embolic complications with bioprosthetics, the rate of structural deterioration over 10 years is substantial in younger patients. Stentless bioprosthetic valves are available and have similar long-term outcomes as stented bioprosthetic valves. Homograft mitral valves, in contrast with homograft aortic valves, do not fair well long term.

Minimally invasive surgery with port systems can be used for mitral valve repair or replacement. To date, there is not a significant clinical advantage to this approach. Robotic surgery is also used, although this remains rare even in developed countries and is nonexistent in the developing world.

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Prognosis

The natural history of mitral stenosis has been profoundly influenced by the advancement of cardiovascular interventions. In most patients, rheumatic mitral stenosis is a progressive disease. In a large referral population without intervention, the mitral valve area decreased at a mean rate of 0.09 cm2/year; however, the rate of mitral valve narrowing in individual patients is variable and cannot be predicted by the initial mitral valve area, mitral valve score, or transmitral gradient, alone or in combination. The mean interval between rheumatic fever and the appearance of symptoms was 16.3 ± 5.2 years. In 84.3% of these patients, death was cardiac-related and due to right-heart failure (27.7%), lung edema resistant to medical therapy (14.5%), thromboembolic (10.8%) or hemorrhagic complications (7.2%), myocardial infarction (9.3%), or infective endocarditis (3.6%); 14.5% of the patients had a sudden death. Progression from mild symptoms to severe disability is typically accelerated and the prognosis dramatically worsens.

In addition to lower rates of restenosis, PMBV and open commissurotomy provided lower rates of reintervention than closed commissurotomy. These results appear consistent with earlier studies. The excellent results, lower cost, and obviation of a thoracotomy and cardiopulmonary bypass advocate PMBV for all patients with favorable mitral valve morphology.

The perioperative mortality rate for mitral valve replacement is less than 5% in young healthy individuals; however, the mortality rate may exceed 20% in older patients who are in NYHA Class IV. Therefore, the procedure should be performed prior to the development of significant left ventricular dysfunction. Despite the increased risk of perioperative mortality, a tangible benefit is derived from mitral valve replacement.

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